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Case Report Anorectal Cancer with Bone Marrow and Leptomeningeal Metastases Ahmed Zeeneldin, 1,2 Nasser Al-Dhaibani, 1 Yasser M. Saleh, 3,5 Amal Mostafa Ismail, 1,3 Zuhair Alzibair, 1 Mohamed Shafi Moona, 1 and Wael Mohamed 4,5 1 Oncology Center, King Abdulla Medical City, Saudi Arabia 2 National Cancer Institute, Cairo University, Egypt 3 Department of Clinical Oncology and Nuclear Medicine, Mansoura University, Egypt 4 Faculty of Medicine, Port Said University, Egypt 5 Oncology Center, Saudi German Hospital, Saudi Arabia Correspondence should be addressed to Wael Mohamed; [email protected] Received 24 June 2018; Accepted 18 September 2018; Published 30 December 2018 Academic Editor: Constantine Gennatas Copyright © 2018 Ahmed Zeeneldin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This is an interesting case of anorectal signet ring carcinoma with rst presentation of an early stage disease, showing the aggressive disease and the undetectable behavior of this type of histology which can mislead diagnosis. Brain/CNS metastasis from colorectal cancer (CRC) is rare occurring in 3% of cases, and leptomeningeal carcinomatosis (LMC) is extremely rare in CRC (<0.02%). Symptoms and signs of LMC are pleomorphic and may be localized to three compartments: cerebral hemispheres, cranial nerves, and spinal cords and roots. Treatment of metastatic rectal cancer has been improving over the last few years with a lot of changes toward longer survival and improvement in quality of life and to change the disease into a chronic condition. However, in our case, the overall survival from the onset of LMC was 3 weeks only. Revising the evidence in the treatment of signet ring histology of rectal cancer, there is no specic treatment recommendation that is for this histology and for such very aggressive behavior which could be considered as a separate entity to the classic adenocarcinoma histology. 1. Case Presentation 1.1. Clinical Data. This is a case of a 42-year-old male with no signicant past medical history. In Feb 2015, he presented with increasing constipation that was later associated with rectal bleeding. In April, there were generalized bone pains involving the chest wall, dorsal spine, and pelvis. PR exami- nation showed a mass almost occluding the lumen located 4 cm from the anal verge. 1.2. Lab. His baseline blood count results are as follows: white blood cells 11.6K/ml, neutrophils 8.4K/ml, hemoglobin (Hb) 12.6 g/dl, MCV 85 , MCH 30 pg, and platelets 202K/ml. His renal and liver function tests were within normal ranges. His baseline carcinoembryonic antigen was 309 ng/dl. Proctocolonoscopy showed a mass 4 cm from the anal canal extending proximally for 10 cm. When biopsied, histopathologic examination result conrmed a poorly dier- entiated adenocarcinoma with focal signet ring morphology arranged in sheets and cords with minimal acinar formation. 1.3. Imaging. Pelvic MRI showed a rectal mass with cir- cumferential thickening and stranding extending to the pelvic side wall (Figure 1) with multiple large left iliac and mesorectal lymph nodes reaching a size of 2.8 cm. Multiple foci of T2 hyperintensity and enhancement were detected involving the lumbar and sacral spine, both iliac bones, and proximal femura. Computerized tomography of chest abdo- men and pelvis showed a rectal mass (9 × 5.6 × 5 cm), left iliac lymph node (1.3 cm), a right upper lung nodule (0.3 cm), Hindawi Case Reports in Oncological Medicine Volume 2018, Article ID 9246139, 6 pages https://doi.org/10.1155/2018/9246139

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Page 1: Anorectal Cancer with Bone Marrow and Leptomeningeal Metastasesdownloads.hindawi.com/journals/crionm/2018/9246139.pdf · 2019. 7. 30. · Case Report Anorectal Cancer with Bone Marrow

Case ReportAnorectal Cancer with Bone Marrow andLeptomeningeal Metastases

Ahmed Zeeneldin,1,2 Nasser Al-Dhaibani,1 Yasser M. Saleh,3,5 Amal Mostafa Ismail,1,3

Zuhair Alzibair,1 Mohamed Shafi Moona,1 and Wael Mohamed 4,5

1Oncology Center, King Abdulla Medical City, Saudi Arabia2National Cancer Institute, Cairo University, Egypt3Department of Clinical Oncology and Nuclear Medicine, Mansoura University, Egypt4Faculty of Medicine, Port Said University, Egypt5Oncology Center, Saudi German Hospital, Saudi Arabia

Correspondence should be addressed to Wael Mohamed; [email protected]

Received 24 June 2018; Accepted 18 September 2018; Published 30 December 2018

Academic Editor: Constantine Gennatas

Copyright © 2018 Ahmed Zeeneldin et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

This is an interesting case of anorectal signet ring carcinoma with first presentation of an early stage disease, showing theaggressive disease and the undetectable behavior of this type of histology which can mislead diagnosis. Brain/CNS metastasisfrom colorectal cancer (CRC) is rare occurring in 3% of cases, and leptomeningeal carcinomatosis (LMC) is extremely rare inCRC (<0.02%). Symptoms and signs of LMC are pleomorphic and may be localized to three compartments: cerebralhemispheres, cranial nerves, and spinal cords and roots. Treatment of metastatic rectal cancer has been improving over the lastfew years with a lot of changes toward longer survival and improvement in quality of life and to change the disease into achronic condition. However, in our case, the overall survival from the onset of LMC was 3 weeks only. Revising the evidencein the treatment of signet ring histology of rectal cancer, there is no specific treatment recommendation that is for thishistology and for such very aggressive behavior which could be considered as a separate entity to the classic adenocarcinomahistology.

1. Case Presentation

1.1. Clinical Data. This is a case of a 42-year-old male with nosignificant past medical history. In Feb 2015, he presentedwith increasing constipation that was later associated withrectal bleeding. In April, there were generalized bone painsinvolving the chest wall, dorsal spine, and pelvis. PR exami-nation showed a mass almost occluding the lumen located4 cm from the anal verge.

1.2. Lab.His baseline blood count results are as follows: whiteblood cells 11.6K/ml, neutrophils 8.4K/ml, hemoglobin (Hb)12.6 g/dl, MCV 85fl, MCH 30pg, and platelets 202K/ml. Hisrenal and liver function tests were within normal ranges. Hisbaseline carcinoembryonic antigen was 309 ng/dl.

Proctocolonoscopy showed a mass 4 cm from the analcanal extending proximally for 10 cm. When biopsied,histopathologic examination result confirmed a poorly differ-entiated adenocarcinoma with focal signet ring morphologyarranged in sheets and cords with minimal acinar formation.

1.3. Imaging. Pelvic MRI showed a rectal mass with cir-cumferential thickening and stranding extending to thepelvic side wall (Figure 1) with multiple large left iliac andmesorectal lymph nodes reaching a size of 2.8 cm. Multiplefoci of T2 hyperintensity and enhancement were detectedinvolving the lumbar and sacral spine, both iliac bones, andproximal femura. Computerized tomography of chest abdo-men and pelvis showed a rectal mass (9× 5.6× 5 cm), left iliaclymph node (1.3 cm), a right upper lung nodule (0.3 cm),

HindawiCase Reports in Oncological MedicineVolume 2018, Article ID 9246139, 6 pageshttps://doi.org/10.1155/2018/9246139

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and no liver metastases. Bone scan confirmed the wide-spread active osseous lesions involving the spine, ribs, andpelvic bones (Figure 2). SPECT-CT suggested diffuse boneinfiltration (Figure 3).

1.4. Treatments and Course. Between June 1 and 14, hereceived palliative radiotherapy to the pelvis in a dose of30 grays over 10 fractions with improvement of the rectalbleeding and was scheduled to start palliative chemotherapy,but the patient became pale and developed progressive andprolonged drop in his hemoglobin and platelet levels(Figures 4 and 5). He received multiple units of packed redblood cell transfusions with no improvements in the hema-tologic parameters. Bone marrow biopsy confirmed thediagnosis of malignant bone marrow infiltration by signetring cells positive for Ck20 and negative for Ck7 withmarkedly reduced hematopoietic cells.

The patient had the height of 159 cm, weight of 69 kg, andsurface area of 1.75. On July 29th, he started zoledronic acid(4mg IV) and capecitabine (1500mg orally twice daily×14 days) (XELOX protocol) as his condition was not fitto receive FOLFORINOX. He required occasional packedRBC and platelet transfusions during the first few daysof capecitabine. Gradually, he started to show clinicalimprovement in the pains and rectal bleeding as well asin the hematological parameters. At the due time of cycletwo on 19/8/2015, his Hb was 8.2 g/dl, platelet was 85K/ml,WBC was 6.2K/ml, and neutrophils were 3.4K/ml. Oxalipla-tin in half its usual dose (i.e., 106mg instead of 212mg) wasadded to capecitabine. Zoledronic acid was also given. Anti-EGFR therapy was not added as RAS testing was not yetreported. Bevacizumab was not considered due to thrombo-cytopenia and the increased risk of bleeding.

At the due time of next cycle on 10/9/2015, his HB was10.5 g/dl, platelets were 109K/ml, WBC was 6.2K/ml, andneutrophils were 4.1K/ml. At that time, he had oral mucositisgrade 2 with dysphagia. Supportive treatment was given, andtreatment was hold. On 21/9/2015, his Hb was 10.6 g/dl,platelet was 159K/ml, WBC was 9K/ml, and neutrophils were7.6K/ml. He showed some improvements of the mucositisand dysphagia. The third cycle was given exactly as thesecond one (i.e., 50% dose reduction of oxaliplatin inaddition to capecitabine and zoledronic acid).

On 29/9/2015, he presented to the Emergency Depart-ment with complained of diplopia and nasal regurgitation.

His vitals were stable. He had left divergent squint. CT brainshowed prominent bilateral hypodense collection more tothe left with some linear opacities and diffuse corticaleffacement (Figure 6). MRI brain showed diffuse meningealthickening and enhancement with evidence of sphenoidaland ethmoidal mucosal thickening (Figure 7). His carci-noembryonic antigen tripled to 1049ng/ml. Radiationoncologists did not encourage the start RT for the fear ofan infectious process. CSF was not tapped. Empirical antimi-crobials were started including antivirals (acyclovir 500mgIV q 8 hours ×14 days and oseltamivir 75mg orally twicedaily for 8 days) and antibiotics (ceftriaxone 2000mg every12 hours for 15 days, levofloxacin 750mg intravenously every24 hours ×5 days, vancomycin 1250mg intravenously every12 hours ×7 days). All microbiological tests were negativeincluding aerobic and anaerobic blood cultures, sputum acidfast bacilli, H1N1 and MERS coronavirus screening, Asper-gillus galactomannan antigen (0.08), serum (s) blastomycesantibody (ab), Brucella abortus and melitensis tests, s. cocciCF and ID, Coxiella burnetii, cryptococcal antigen (ag),serum histoplasma ab, and Syphilis TP. Patient did notshow signs of improvements. Later, high-resolution CT chestshowed two right lung nodules and the largest is 0.5 cm indiameter. CT abdomen and pelvis showed progression of rec-tal lesion and newly developed innumerable small hypodenseliver lesions of 0.7 cm diameter. The patient ran a gravecourse and expired on 17/10/2015.

2. Discussion

Worldwide in the year 2012, colorectal cancer (CRC) isthe third most common cancer in males and the secondin females. It is the fourth cause of cancer death in malesand the third in females. In Arab countries, CRC is thefirst common cancer in males and the second in females.It is the second cause of cancer mortality both in malesand females [1, 2].

Histologically, the WHO classified colorectal carcinomainto adenocarcinoma (AC), medullary carcinoma, mucinousAC, signet ring cell carcinoma (SRCC), and some othersubtypes. In mucinous AC (MAC), >50% of the lesion isextracellular mucin, and in SRCC, >50% of the tumor issignet ring cells with prominent intracytoplasmic mucin[3]. Almost 96% of SRCC originate in the stomach and therest in the colon, rectum, pancreas, urinary bladder, andbreast [4]. SRCC constitutes 1.1% of colorectal cancers [5].

Colorectal SRCCs are present at an advanced stage withT3 or T4, positive LN, and distant metastases. They havepoor survival [5, 6]. They are prognostically unfavorableindependent of the stage [3]. Compared with AC, colorectalSRCC tends to occur at younger age, to affect the right side,to be poorly differentiated, to recur more, and to have poorsurvival [5, 6]. They express mucin-related genes (HATH1,MUC2, and SOX2) and show disruption of the E-cadherin/beta-catenin complex, amplification of Bcl-2 [6], low K-ras,high BRAF mutations, and high MSI [7]. Loss of proteinexpression of E-cadherin may contribute to the high-gradeand invasive nature of colorectal SRCC [7]. In the currentcase, the patient was young (42 years) and had anal/rectal

Figure 1: MRI showing the rectal lesion with the perirectal fatstranding.

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Rt lat skull Ant chest Ant pelvis

Figure 2: Bone scan showing the widespread osseous deposits.

Figure 3: SPECT-CT showing diffuse bone and bone marrow lesions.

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Figure 4: Graph showing the hemoglobin (g/dl) and white cell count (K/ml) of the patient during the disease course.

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lesion that is locally advanced (T3) associated with distantmetastases. He ran a rapid grave course.

Skeletal metastases (SKM) in CRCmay reach up to 24% ifradiotherapy or systemic therapies are not used [8] and to5.5–11% when these therapies are used [9–11]. IsolatedSKM is rare, occurring in 1–2% of CRC [8]. It is usually asso-ciated with liver or lung metastases [8, 9]. SKM is more inyounger patients, in rectum and caecum primarily, and inSRCC [8–10]. CRC SKM affects the vertebral column in

65%, hip/pelvis in 34%, long bones in 26%, and other bonesin 17% [10]. SKM usually presents with bone pains or path-ological fractures [12]. Time from CRC diagnosis to onsetof SKM ranges from 10 to >5000 days with a median of11 months [10]. Skeletal scintigraphy detects SKM withhigh sensitivity. Palin X-rays are helpful in symptomaticlesions and in assessing fracture risk or questionable scinti-graphic findings. CT is helpful when other imaging tech-niques are unclear. Whole-body MRI and PET-CT are themost sensitive and specific methods for the detection ofSKM. Hybrid techniques like SPECT-CT, PET-CT, andPET-MRI combine the strengths of their different compo-nents and avoid the weaknesses [13]. Traditional treatmentsfor SKM include radiation, surgery, and chemotherapy [14].Both denosumab and zoledronic acid reduce pains andskeletal morbidities in patients with SKM [12, 15]. In 5 years,38% of patients isolated SKM are alive compared to 16%when other metastases coexist [11]. The median survival is5–7 months [10, 16]. In the current case, SKM was the initialsite of metastasis and developed 4 months following initialdiagnosis. It presented with bone pains and tenderness andconfirmed by bone scintigraphy and SPECT/CT. He receivedpalliative RT, zoledronic acid, and systemic chemotherapywith mild improvement. The overall survival from the onsetof SKM was 5 months.

Bone marrow metastasis (BMM) was noticed at necropsyin 93/1541 CRC patients (11.6%) where chemotherapy wasrarely used. It is extremely rare (<1%) in the absence of liverand lung metastases and increases to 3% with both liver andlung metastases [17]. The most common metastatic siteassociated with BMM from solid tumors is the bone in 70%of cases followed by liver (14%), brain (10%), and lung(10%) metastases [18]. Early features of BMM include micro-angiopathic hemolytic anemia and leukoerythroblastosis in70% of cases. Clinically, patients present with anemia in68%, thrombocytopenia in 58%, and neutropenia in 23%.Bicytopenia is encountered in 32% and pancytopenia in18%. About 15% of cases had no hematological findingsand were suspected based on imaging only [18, 19]. Usingmodern techniques, malignant cells were found in BM in21% of patients with stages I–III at the time of curative sur-gery [20]. However, the clinical relevance of micrometastasisin BM is to be validated. Mostly, its value may be limitedunless supported by some other clinical findings, such as aleukoerythroblastic reaction or abnormal peripheral bloodcounts [21]. Despite BM biopsy is the surest and fastestmethod of diagnosis, MRI and FDG PET or PET/CT are verysensitive in the detection of BMM [21, 22].

BMM from CRC is primarily treated by chemotherapywith or without targeted therapy. Agents most commonly

Figure 6: MRI showing leptomeningeal thickening.

Figure 7: MRI showing sphenoidal and ethmoidal mucosalthickening.

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Figure 5: Graph showing the platelet count (K/ml) of the patient during the disease course.

4 Case Reports in Oncological Medicine

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used are fluoropyrimidines (5-FU, S1) and oxaliplatin andoccasionally bevacizumab. These lead to clinical improve-ments in many patients [23–28]. Cytopenias secondary toBMM not only increase the risk of infection and bleedingbut also hinder the delivery of effective chemotherapy [18].BMM usually carries a poor prognosis with a median survivalof 5–7 months [29]. Performance status, other metastaticsites, and platelet counts are important prognosticators.Survival of patients with thrombocytopenia is shorter thanwith normal platelet counts (1 month vs. 13 months) [18].

Brain/CNS metastasis from CRC is rare occurring in3% of cases [10]. Leptomeningeal carcinomatosis (LMC)is extremely rare in CRC (<0.02%) [30]. It is rarely thesole site of intracranial disease [31]. Symptoms and signsof LMC are pleomorphic and may be localized to threecompartments: cerebral hemispheres, cranial nerves, andspinal cords and roots. Headache, diplopia, and back/neckpain are common. CSF cytology is the gold standard inLMC diagnosis. Although CSF cytology has 75% sensitivityand 100% specificity, it has a low negative predictive value.CT scans are abnormal in 25–56% of cases with LMC.However, contrast-enhanced MRI has higher sensitivity(59%) and specificity (95%) [32]. Without treatment, themedian survival of patients with LMC is 4–8 weeks.Patients usually die of progressive leptomeningeal or sys-temic cancer [30, 32, 33]. Bulky leptomeningeal disease, con-current CNS disease, epidural cord compression, and poorperformance status are poor prognostic factors [32]. Intra-thecal or systemic chemotherapy may be used with limitedefficacy [34]. In the current case, LMC was suspected clini-cally based on the neurological findings (diplopia and squint)and MRI. However, the concomitant mucosal thickening ofthe paranasal sinus raised the issue of secondary meningitis.However, the lack of response to a multitude of antimicro-bials was going with LMC. The overall survival from theonset of LMC was 3 weeks.

Conflicts of Interest

This is a case which was reported during our work in thehospital, and there are no direct financial, indirect financial,and career or personal belief conflicts.

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